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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Control of viral replication after cessation of HAART. | Van Gulck et al. AIDS Research and Therapy 2011 8 6 http www.aidsrestherapy.eom content 8 1 6 AIDS RESEARCH AND THERAPY CASE REPORT Open Access Control of viral replication after cessation of HAART 1 1 1 1 234 Ellen Van Gulck Leo Heyndrickx Lotte Bracke Sandra Coppens Eric Florence Anne Buvé Paul Lewi Guido Vanham1 5 Abstract We describe two patients who did not experience a viral rebound after cessation of HAART which was initiated for progressive disease. CD4 T-cell count remained stable in one patient and progressively declined in the other despite apparent viral control. We failed to identify any immune activation or genetic markers that could offer an explanation for this unusual secondary controller status. But their viruses are clearly less fit compared to viruses from rebounders. Introduction Highly active antiretroviral treatment HAART has improved life expectancy and quality of life of HIV infected patients 1 . However so far it is not possible to cure HIV infection mainly because latent reservoirs persist even in patients who are on effective combination treatment 2 . Cessation of HAART results in viral rebound within days or weeks and pre-treatment levels of viral load VL are typically reached within one year after treatment interruption 3 4 . In 2008 we identified a patient who after stopping HAART had a VL below the detection limit of 1 6log for more than 2 years. After searching the data base of 1 700 HIV infected patients under follow-up at the clinic of the Institute of Tropical Medicine another patient was identified who spontaneously controlled VL after cessation of HAART for at least 6 months. We labeled these two patients secondary controllers SC as opposed to elite controllers EC who spontaneously control viral replication but are treatment naive. Comparison between SC and rebounders Methods In order to identify correlates of SC status we compared clinical characteristics viral factors genetic traits and immune activation markers in the two SC
